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Vive Revista de Salud

versão impressa ISSN 2664-3243versão On-line ISSN L:2664-3243

Resumo

CALDERON CALLE, Fanny  e  PRIETO FUENMAYOR, Carem Francelys. FTL3-ITD mutation and its relationship with hematological and clinical variables in individuals with Acute Myeloid Leukemia. Vive Rev. Salud [online]. 2021, vol.4, n.10, pp.128-142.  Epub 30-Abr-2021. ISSN 2664-3243.  https://doi.org/10.33996/revistavive.v4i10.81.

Introduction.

Acute Myeloid Leukemia is the most common hematological neoplasm, characterized by an uncontrolled proliferation of hematopoietic stem cells. The FLT3 / ITD mutation occurs in approximately 30% of all patients with this pathology, it is associated with a higher risk of relapse and lower survival. FLT3-ITD can be used as a poor prognostic factor, important for predicting clinical outcomes in patients with AML.

Objective.

The objective of this study was to characterize the FLT3 / ITD mutation and its relationship with hematological and clinical variables in patients diagnosed with Acute Myeloid Leukemia treated at SOLCA in the city of Cuenca, period 2013-2020.

Methods.

Data were obtained from secondary records in a hospital database, the universe of the sample was made up of 63 patients, diagnosed with AML, and the FLT3 / ITD mutation was analyzed by Conventional PCR.

Results.

The presence of the mutation was found in 9.5% and a statistically significantly association with hematological alterations related to abnormal hemoglobin levels (p = 0.037) and ratio 6.63 and LDH elevated in 1.21 times (p = 0.024); Elevated leukocyte and blast count (p = 0.031). Individuals carrying the mutation had a higher incidence in males and in the middle adult age group (45-64 years). Conclusions. The international literature affirms that the FLT3 / ITD mutation is an important prognostic marker; Due to its low frequency, it was not possible to determine a statistically significant relationship with other clinical variables in our study, for which it is suggested to expand the unirverse of the sample.

Palavras-chave : Internal Tandem Duplication; Leukemia Myeloid Acute; Lactate dehydrogenase; Tyrosine kinase.

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